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It happens every week. Typically around 3pm on Tuesday afternoons when I'm wrapping up a clinic visit. I'll have this sensation ominously run through my body. It starts with the feet. They becomes restless with tapping which eventually progresses to sitting up on my toes while on the stool in the room. Then it'll methodically move up to where I engage my quads. With my legs growing more tense by the second I finally end the ritualistic act by kicking in the glutes and engaging the entirety of my lower body all the while sitting on the stool. This is me running late to my next visit. This is me needing to be somewhere else. This is me not being focused on my patient but the clock. It's inevitable.

One of my earliest memories of sitting with intention is also my favorite. I remember watching What Dreams May Come as a teenager and finding the end to be profoundly romantic. I still do. For better or worse, being willing to sit with another in hell to just be near them was a thought that I continued to carry on into future relationships. Love to me is less about sharing happy experiences but having the desire to sit with someone in their hell for long enough that it could potentially become yours as well.

It's not sound reasoning as there are many scenarios I can envision being fraught with something confused with love (domestic violence, mental illness, addiction, etc) but to me it's still the pinnacle of what a relationship can be. Of course in the movie, the sacrificial act is enough to bring the protagonist's wife out from hell but there isn't always a happy ending and that's part of what makes the act so potent.

Physicians use the phrase "walk with our patients" quite a bit. It's quickly working its way back into the receptacle of exhausted mantras such as "being a change agent" and "culture of _____" but it's used for a good reason. It's a great visual. A physician slowly walking down a road with their patient, grabs their hand, then says "your hemoglobin A1c will improve from 6.6 to 6.3 as I walk this journey with you!"

But often as humans, not just patients, we don't have the luxury of walking.

At one's nadir, we're often not walking or even crawling but in fact sitting. When you are given a grave diagnosis, you have to sit with it. When depression is at its worst, you're having to sit with it. There will always come a time during someone's grief or misfortune where there will be no forwards or backwards, just an uncomfortable sitting in neutral. As a physician, I can honestly say that I find the prospect of walking or running much more appealing as it exudes thoughts of good health and progress. But I've come to recognize in my patients' lives as well as in my own that the people who are willing to patiently sit with you in the darkness are often the most significant.

This imagery of sitting in darkness was recently rekindled as I have attempted to do my own self-work with race, implicit bias and reconciliation. Back in 2015, Allen Belton, Senior Partner of Reconciliation Ministries at Breakthrough Partners, spoke about reconciliation at my church. He again conjured up thoughts of sitting as he remarked that "in order for reconciliation to truly occur, people must be willing to sit with each other in the pain of the past." Healthcare providers are probably worse than most when it comes to wanting answers immediately. We see a problem and we want to fix it. The thought that the solution would be to continue on in the same space is one we tend to struggle with as a whole.

This all runs somewhat contrary to the recent movement to stand more during the day. Yes, evidence is growing that should encourage all of us to stand more during the day. Certainly this is a good idea for physicians when charting alone or at other times of the day but it will never be my choice when in a room with a patient. The time is too short and the moments too precious to let someone think anything other than the other person in that room is present and willing to sit in the pain.

Scenario 1:

Chief Complaint: 32 year old non-pregnant female, non-smoker, occasional alcohol use, no significant past medical history presenting with dyspnea and reports of lower extremity edema. I give you the following tools:

Physical exam

CXR

EKG

Pro-BNP

Framingham Heart Failure Diagnostic Criteria

You don't get to choose an echocardiogram (too easy)

Which ones do you want to use for your evaluation if you're at all concerned about CHF (which you're probably not), specifically systolic CHF (HFrEF)?

Scenario 2:

Chief Complaint: 57 year old male, 30 pack year smoker, moderate alcohol use, past medical history significant for hypertension, diabetes and hyperlipidemia presenting with dyspnea and reports of lower extremity edema. I give you the following tools:

Physical exam

CXR

EKG

Pro-BNP

Framingham Heart Failure Diagnostic Criteria

You don't get to choose an echocardiogram (too easy)

Which ones do you want to use for your evaluation if you're at all concerned about CHF? (which you probably are)

Best Practice Answer:

I recently gave a talk on outpatient CHF management and the answer to these scenarios surprised me. I have thought for many years now that the CXR was something that docs ordered blindly without reason in suspected CHF cases. Now that may still be the case but at least they have some good data to back them up. At the same time, Pro-BNPs are becoming more and more of a regular occurrence in diagnostic work ups and they're really best suited for only one side of the CHF equation.

Taking a look at the likelihood ratios compiled below from a 2012 AFP article we can see that the strategy for ruling IN CHF is not the same as ruling OUT CHF.

The healthy 32 year old female has a low pre-test probably of having CHF because of the low prevalence in her specific cohort (young and healthy). Remember that prevalence affects likelihood ratios. We're going to want to use strategies with low negative likelihood ratio (-LR) to rule out the small chance she has CHF. As you can see above, the Framingham criteria for heart failure (especially systolic heart failure) as well as a reduced Pro-BNP level (typically < 300) have a low -LR and would be great tests to use in this case. Hard time remembering how to make a diagnosis with the Framingham criteria? Just remember that if you can make $1 between the two lists you have a diagnosis (see below). One final thing I would add is that EKG's are excellent at ruling out systolic heart failure if normal (98% NPV). [1] Just don't rely on them to rule anything in or rule out diastolic heart failure.

Now what about scenario 2? Use the opposite logic. A patient who has a HIGH pre-test probability of CHF (smoker, hyperlipidemia, older) can more accurately be ruled IN for the diagnosis with a higher positive likelihood ratio (+LR). So in this case I would reach for some rather easy physical exam findings (S3, displaced cardiac apex) and the aforementioned CXR. Remember though that the findings you're looking for are interstitial edema (Kerley B lines) and pulmonary edema. As you can see further down the list, cardiomegaly and pleural effusion don't help you as much.

An interesting side note is how low many of the signs and symptoms we normally report are in the list. Crackles, peripheral edema, PND and orthopnea are all rather low on the list for +LR.

What Saves Lives in Systolic Heart Failure?

Flavor 1: ACE Inhibitors

Flavor 2: Beta-blockers

ACE inhibitors and beta blockers share lots of similarities. They both have a substantial amount of old but credible data to back them up. They both have been found to improve function (NYHA classification) in patients with systolic heart failure (HFrEF) . They both show improvement in all-cause mortality. [2,3,4] You should use both of these any chance you get in your HFrEF patients. Long term outcomes aren't affected by which one you start first but some would argue to start the ACE inhibitor first due to beta blockers potentially causing further acute decompensation.

Flavor 3: Mineralcorticoid Receptor Antagonists (Spironolactone)

Once your patient is already titrated up on the above medications you should begin thinking about additional therapies if their function isn't optimized (NYHA 2-4). MRA's have been shown to improve all-cause mortality, hospitalization rates, and function status in those already on medical therapy. You want to remember to check the potassium since it's potassium sparing. American Heart Association (AHA) has the unrealistic monitoring schedule recommendation of 2-3 days after starting therapy, 1 week after, then monthly for 3 months then every 3 months after that. Just food for thought.

Flavor 4: ARNI's

Angiotensin Receptor-Neprilysin Inhibitors. Mouthful. These guys are a combo drug with Sacubitril and Valsartan. You already know what Valsartan does. Sacubitril is the Neprilysin inhibitor. What is Neprilysin? It's an endopeptidase that cleaves vasoactive peptides such as BNP. The rationale is to inhibit the inhibitor to ensure a healthy amount of BNP is floating around to vasodilate. Newer RCTs have found a reduction in all-cause mortality and hospitalization rates BEYOND ACE inhibitors. [5] The indications can be somewhat narrow though. Recommendations are to consider ARNI's if the following criteria are met:

LVEF < 40%

Elevated BNP or heart failure hospitalization in past year

SBP > 100

GFR > 30

Those who have tolerated ACE inhibitor in the past

If that sounds like one of your patients this might be a consideration but just remember that ACE inhibitors have years of good data showing improvement in patient centered outcomes while ARNI's haven't had quite that amount of data to back it up.

Flavor 5: Cardiac Devices

I won't go into too much detail here as placing ICDs and CRTs don't quite fit my scope of practice. But it's important to remember that cardiac devices have been shown to improve outcomes in certain subgroups of patients. Specifically, they have been shown to improve all-cause mortality compared to medical therapy [6]. These results have ranged anywhere between 28-53% improvement based on which type of device was studied. CRT-D was found to have the largest mortality benefit. What is CRT-D vs CRT-P vs ICD? Good question since I didn't know the difference myself beforehand. Here's the breakdown:

ICD: Lead in right atrium and right ventricle. Used to shock abnormal rhythms.

CRT-D: Lead in right atrium, right ventricle and left ventricle to help synchronize the pumping of blood to the rest of the body. These include an ICD as well.

CRT-P: Same as the CRT-D except without the ICD.

What patients receive the most benefit? The 2012 AHA recommendations are divided by classification of recommendations (1-3) and level of evidence (A-C). Here are the Class 1, Level A recommendations:

Quick Shout Out

I didn't discuss treatment modalities that improve morbidity but there are a number of these as well for systolic heart failure. These include digoxin, immunizations (flu, pneumococcal), diuretics, and cardiac rehabilitation. There was subgroup analysis from the DIG trial previously that did show some mortality benefit for digoxin when those patients were within the 0.5-0.8 ng/mL range for serum digoxin concentration. The downside is that when this level increased above 1.2 there was actually an increase in mortality rates. It's also just a tricky medication to use overall that requires close monitoring.

You Forgot Diastolic Heart Failure (HFpEF)!

You're right. I didn't mention diastolic heart failure since there is no substantial evidence to show any mortality benefit in any specific treatment option. Exercise training is the only intervention to show improvement in quality of life and exercise capacity [7]. Unfortunately neither Medicare or Medicaid cover this for diastolic heart failure. So we're stuck with symptom management and contributing factor management for treatment.

So remember next time you want to rule IN someone with a high likelihood of CHF go for the CXR and cardiac exam. If you want to rule OUT someone with a low likelihood of CHF go for the Pro-BNP, Framingham Heart Failure Criteria, and potentially an EKG. Once you make that diagnosis you can reach for your five lifesaver flavors to help improve mortality rates for your patients.

Click Me!

Quick plug for my new podcast Greyscale. It can be found on iTunes or anywhere you like to get your podcasts. Two episodes currently up with a third on the way. I'll also be launching a Sports Medicine Podcast (The Break) in the near future as well!

The first words of my last blog post were “I’m still alive”. Well, I’m happy to report 470 days later that I am indeed “still alive”. I’ve had a bit of a hiatus since last. A lot has happened. I had a very memorable but next-level busy Chief year. I graduated from residency (shout out to Class of '15). Then I was fortunate enough to land my “dream job” as faculty member at Swedish First Hill. Hopefully I can get back into the groove of writing more now. If not, my next post might be sometime in 2016 (actually, it’s highly likely it’ll be in 2016).

Speaking of staying alive, sometimes the only thing you can do to keep living is to continue to just breathe. It's a bit of a played out sentiment that you're likely to see on a motivation poster featuring a kitten. But sometimes it can take on more like a Pearl Jam concert in Seattle. Occasionally that breathing can be an indication for what’s going on beneath the surface. A sigh. A deep breath. They all mean something. But today I'm looking into different types of breathing patterns, what they look like, and what could they potentially represent.

Before we look into abnormal patterns of breathing we should probably go back to year two of medical school and review exactly what happens with normal breathing patterns. Feel free to skip the next two paragraphs if it’s old hat to you. When you take a deep breath in, air travels down your upper airway down to your lower airway. The upper airway serves as a filter for various particles in addition to humidifying and warming. Once the gases reach the lower airway it’s primarily about gas exchange. You want the oxygen. You don't want the carbon dioxide. Remember that the lungs have a dual blood supply. You have your pulmonary circulation, which sends deoxygenated blood through the pulmonary arteries to your lungs. Once at the lungs, gas exchange occurs at the capillary bed and sends oxygenated blood back to the heart via the pulmonary vein. On the other end you have your bronchial arteries that arise from the descending aorta to supply blood to your lung parenchyma.That’s the basics about blood supply.

How about the mechanism for getting the air in and out of the lungs? Respiration is controlled by a group of muscles – “the muscles of respiration”. Your diaphragm is the major player in this along with the accessory muscles (sternocleidomastoid, scalenes, and intercostals – aka the muscles we look at when evaluating for retractions). These muscles will help expand the lung which creates a negative intra-thoracic pressure gradient that helps bring the air down to the lower respiratory tract. Once you finish that breath you take in your vital capacity (remember VC + RV = TLC) and enter expiration. Expiration is a passive process which is essentially a function of the elastic recoil of the lung and chest wall.

All right. Out with the normal, in with the abnormal.

*Disclaimer: Some of the videos below don't have explicit patient approval listed by the publisher and others may be disturbing to watch. Please watch at own discretion*

KUSSMAUL BREATHING

Eponym Source: Old white guy in the late 19th century writing about diabetic coma.

Otherwise known as “air hunger”, key findings in Kussmaul respirations are RAPID and DEEP labored breathing with an urge to breath deeply. The rate can be anywhere from slow, normal, or fast. This is due to the patient having metabolic acidosis. When you have low bicarbonate in the blood you will try to compensate for it in the acute period by “blowing off” more carbon dioxide. So with the onset of hyperventilation your ABG will normally show a metabolic acidosis with attempted compensatory respiratory alkalosis. The most common scenario to see Kussmaul respirations is indeed in DKA like the video depicts but it can happen in any scenario where you have a patient with metabolic acidosis. Fun fact: you can reproduce the effect, to a degree, by rapidly breathing in the air in a recently-emptied plastic soft drink bottle which contains an elevated amount of carbon dioxide.

CHEYNE-STOKES RESPIRATIONS

Eponym Source: Two old white guys in the 19th century who described the breathing of a 60 year old man with CHF and stroke.

Also known as “periodic respiration”, Cheyne-Stokes (CS) respirations are characterized by a gradual hyperpnea followed by gradual hypopnea and eventually a period of apnea. In other words, the patient will gradually take deeper breaths (potentially faster as well) then will slowly take more shallow breaths until they reach a period where they don’t breath. The entire cycle takes anywhere between 30 seconds to 2 minutes and the apnea portion will normally last anywhere from 10-20 seconds. The mechanism behind CS respirations is that the apnea (caused by a number of etiologies) will lead to a build up of carbon dioxide which then leads to a disporportionate compensatory hyperventilation which then leads to the apneic phase again. This type of breathing pattern can be seen in CHF, strokes (or any other CNS insult), hyponatremia, carbon monoxide poisoning (important for the cold winter months), excessive morphine dosages, syncope and coma. Most notably, CS respirations are sometimes seen in patients who near death.

BIOT RESPIRATIONS

Eponym Source:Old white guy in the 19th century who wrote of a 16 year old patients with TB meningitis.

Biot respirations can be thought of as the atrial fibrillation of breathing. The correct definition is a breathing pattern of markedly variable tidal volumes and random apneas with no regularity. Occasionally you will see Biot respirations described as regular, rapid, shallow breaths followed by apnea but that’s really more of a definition of “cluster breathing”. Biot respirations are seen more often in CNS insults such as stroke or trauma. It can also be occasionally seen with chronic opiate use as well.

AGONAL BREATHING

Many people will go through life never to know their true purpose. Fortunately for these three men, they found their calling and it was to film the next three videos. These thespians offer a tour de force portraying agonal breathing. I found it hard to rank these but I believe I have accumulated enough objective differences to find a true winner.

In third place is Maroon shirted man in “Nice Rug, Bad Drugs” where he depicts a struggling Persian rug salesman who overdoses on heroin and subsequently incurs an intracranial hemorrhage after falling from a stack of rugs late at night. I put this one in third place since there was no footage from a standing position to the agonal breaths. It’s well known in the agonal breathing youtube video community that a proper depiction will always show the moments leading up to the event. I do think he offers a unique perspective though as his breaths contain a substantial amount of phlegm. Something the other actors fail to provide.

It was a close battle for first place but the runner up goes to WA Gaspen for his performance in “Extinguishing Life”. The older gentleman offers a complete picture from carrying the extinguishers to the fall and subsequent agonal breaths. Unfortunately, I thought his fall was a bit soft as he braced quite heavily with his left hand. In addition, his breaths although quite dramatic complete with exaggerated mouth movements, was a bit premature. He begins these breaths almost immediately after hitting the ground. One would expect a bit more of a tempered approach by such a veteran.

And the winner is…

Ron Straight in “Blue Wall, Blue Shirt, Blue Face”. A quick google search shows that Ron has been a paramedic and teacher in Vancouver, CA for 30 years. Without a doubt, Ron’s entire life built up to this exact moment where he seized the spotlight and delivered a memorable performance. Ron played a decorated veteran who took up playing the blues in New Orleans. While waiting for his moment to finally take the stage, Ron succumbed to an untimely death. We all remember his final words in the film, “I just want to sing the blues. It doesn’t mean I’m blueee…. *gurgle*” (not depicted) He sealed the deal with his heart wrenching 6 second seizure after falling to the floor with abandon.

Honestly, after watching those three videos you can get a good sense of what agonal breaths entail. They can be quite variable but will typically have gasping, occasional myoclonic jerks, episodes of apnea and labored breathing with no particular sequence. This can be seen in cardiac arrest/cardiogenic shock as well as strokes or trauma that damage the medulla oblongata. Definitely a poor prognosis when you see this type of breathing and you should probably be less focused on the breathing when you encounter it and more on the impending catastrophe that is likely occurring.

One thing I didn't write about was treatment. The reason is that the treatment will always be the same. Whenever you come across an abnormal breathing pattern it's most likely a response to what's happening internally. Treatment will always be to correct the internal disturbance (CNS, cardiac, metabolic, etc).

So that's abnormal breathing in a nutshell. Just another reminder that there's always more going on than what you can see on the surface. Also that you're never too old to pursue your dreams. Just look at the three guys above.

Shameless Plug: If you're in the Seattle area and have nothing to do on December 11th come check out our residency band, Plan B, as we do a benefit show to help raise money for our Global Health Program! Click here for the Facebook invite. If you can't make it consider donating to the program found at the facebook event page. Thanks!